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Results for “FOLIC ACID DEFICIENCY”

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At least 559 records · Page 31Linked to original sources
PubMed1995

[Celiac disease in adults revealed by sensory-motor neuropathy].

Central or peripheral nervous system complications are occasionally observed in adult patients with celiac disease. Several mechanisms have been proposed including vitamin deficiency, vascular inflammation and a direct effect of gluten intolerance. Typical nerve fiber damage due to demyelinization has been suggested. We observed a 65-year old woman with a right peroneal nerve palsy superimposed on a diffuse peripheral neuropathy who was found to have folic acid deficiency which in turn led to the diagnosis of adult celiac disease. Electrophysiological and histological studies demonstrated a predominantly demyelinating peripheral neuropathy which responded first to parenteral folic acid supplementation and second to a gluten-free diet. The mechanisms of peripheral nerve damage in adult celiac disease are briefly discussed and the possible role of folic acid deficiency is emphasized.

Aged↗
PubMed1978

Megaloblastic erythropoiesis and tissue depletion of folic acid in the cat.

Dietary requirement for folic acid was shown in the cat. Folic acid deficiency was produced by feeding young cats a deficient diet (0.125 mg of total folate/kg of dry weight by analysis) for 22 weeks. The folic acid-deficient cats grew normally, but had reduced plasma, red blood cell, and liver folate concentrations in comparison with those concentrations in cats fed a control diet (1.36 mg of total folate/kg).. Urinary excretion of formiminoglutamic acid was increased in all deficient diet cats 24 hours after L-histidine injection. Erythroblasts in bone marrow smears from folic acid-deficient cats were megaloblastic; they showed abnormal nuclear chromatin patterns and had nuclear-cytoplasmic asynchronism.

Animals↗
PubMed1966

Plasma lactate dehydrogenase in megaloblastic anaemia.

Raised plasma lactate dehydrogenase (LDH) values were found in 26 patients with marked megaloblastic anaemia due either to vitamin B(12) or folic-acid deficiency or a combination of these factors.Minor megaloblastic changes were not usually accompanied by plasma LDH elevation. Serial LDH estimations were as valuable as serial reticulocyte counts in assessing the response to physiological doses of folic acid and therefore in deciding whether megaloblastic anaemia is partially or completely due to folic acid deficiency.

Anemia, Macrocytic↗
PubMed1988

Folic acid therapy for alopecia in a Charolais calf.

A three-week old male Charolais calf which had a history of progressive hair loss and clinical signs, including crusts and brown patches similar to those in folic acid deficiency syndrome in man, was subjected to folic acid therapy. Daily oral administration of folic acid (1 mg/kg/day) resulted in the gradual disappearance of the crusts and patches within two weeks and a steady growth of hair and recovery to a normal state within two months. Folic acid, which is required for cellular turnover in a variety of tissues and organs including the hair follicle, may serve as an effective therapeutic agent in some types of alopecia triggered by a deficiency of either folic acid or the co-enzymes involved in the synthetic pathway of DNA.

Alopecia↗
PubMed2005

Folic acid and colorectal cancer prevention: molecular mechanisms and epidemiological evidence (Review).

Epidemiological studies suggest that a diet rich in fruits and vegetables protects against colorectal cancer. This effect may result from their high levels of folic acid (pteroylglutamic acid). Folic acid holds a key position in DNA synthesis and mitosis as well as DNA methylation and regulation of gene expression. Folic acid deficiency has been associated with site- and gene specific DNA hypo- and hypermethylation. Furthermore thymidylate synthesis is restricted by folic acid deficiency which causes misincorporation of nucleotides and DNA strand breaks. Much epidemiological evidence supports the hypothesis that insufficient folic acid supply favors the development of colorectal tumors, particularly prospective studies have supported this connection. However, the data from case-control studies are less consistent. Functional polymorphisms in folate-metabolizing genes, especially the methylenetetrahydrofolate reductase (MTHFR) are capable of modifying the risk of colorectal cancer. Observational studies show that individuals with the homozygote genotype for the MTHFR (677C-->T) polymorphism are at higher risk when folic acid supply is low. Currently there are only few human intervention trials which show that folic acid can modify and inhibit the development of colorectal tumors. Additional studies are required in order to determine whether folic acid will be a useful agent in colorectal cancer prevention.

Adenoma↗
PubMed1985

[Course of epilepsy in patients who have suffered adverse effects of anticonvulsant preparations according to the results of long-term follow-up].

The author studied 99 epileptic patients in whom 5-10 years ago anticonvulsants had caused side-effects. In 10% of the patients, a stable remission of the paroxysmal manifestations and an improvement of the mental status was achieved after controlling the complications. The majority of the patients exhibited slow progression of the epileptic process following a reduction of disturbances induced by intoxication and folic acid deficiency. Severe toxic, metabolic and allergic complications (30%) were followed by further considerable progression of the paroxysmal and psychopathological symptomatology. The degree of progression and severity of the organic brain lesion in epileptic patients is an important factor affecting the manifestation of the side-effects associated with anticonvulsants and the efficiency of further anticonvulsive therapy. In 4% of the patients the author observed repeated drug-induced complications. The prophylaxis of repeated complications of the anticonvulsant treatment prevents epilepsy aggravation.

Adolescent↗
PubMed1998

Sulfadoxine-pyrimethamine embryopathy in Wistar rats.

Pregnant Wistar rats received a therapeutic dose (0.72 mg/kg body weight) of intramuscular sulfadoxine-pyrimethamine on days 5, 12, and 19 of gestation. The treated animals showed elevated neutrophilic lobe average and increased urinary excretion of formiminoglutamic acid (FIGLU) as compared with controls (p < 0.001), confirming folic acid deficiency due to sulfadoxine-pyrimethamine treatment. Complete embryo resorption occurred in the treatment group, while the control animals littered normally. These findings imply that sulfadoxine-pyrimethamine should be used with utmost caution in early pregnancy as this regimen can lead to folic acid deficiency and consequent pregnancy wastage.

Animals↗
PubMed1966

Correlation of peripheral white cell and bone marrow changes with folate levels in pregnancy and their clinical significance.

Two hundred and thirty-eight ;megaloblastic' pregnancies are reviewed. Bone-marrow aspiration was performed in every case. Serum folate estimations were strongly suggestive of folic acid deficiency in only 34% of cases. If, however, the red cell folate was determined as well, there was an almost complete agreement with the changes in the erythroblasts. It is suggested that hyper-segmentation of the neutrophils in association with a diminished red cell folate level is indicative of significant folic acid deficiency. This series possibly shows a slight but statistically insignificant increase of accidental haemorrhage. No effect on birth weight or incidence of stillbirth was demonstrable.

Adult↗
PubMed2001

[Colonic aganglionosis with ileal involvement. Ileocolic plasty].

During 1994 through 1999, we have treated five patients (3 boys, 2 girls) with total colonic aganglionosis (TCA) and ileal involvement. In three of them we performed a diverting ileostomy in the neonatal period and at the age of four and five months respectively in the remaining two patients, due to intestinal obstruction. In these two last patients a diagnosis of Hirschsprung's disease was made by anorectal manometry and rectal biopsies in the neonatal period. During laparotomy, a cutaneous ileostomy was created in all patients at the distal end of normal ileum, which was 30 to 110 cm (mean = 71 +/- 37 cm) from the ileocecal valve. After operation, a short bowel syndrome developed in three patients causing fluid and nutritional problems that required prolonged total parenteral nutrition (TPN). The definitive operative repair is performed at 4.5 to 14 months (mean = 8 +/- 3.7 months) by a 12 to 20 cm side-to-side ileocolostomy created between the ileum and aganglionic ascending color (Boley procedure) and ileorectal primary anastomosis (Rehbein procedure) using a circular stapler. Rectal dilatation, irrigation of the colon with saline, loperamide hydrochloride and resincholestyramine were begun in all patients postoperatively. Oral antibiotic prophylaxis, was given to the three patients who suffered from SBS. Oral feedings with semielemental diet were tolerated once stools were semiformed and TPN was discontinued at 8 to 34 days (mean = 21 +/- 1.7 days). postoperatively. After the definitive operation, enterocolitis developed in two patients, requiring one of them a short hospitalization during the episode. A possible explanation for the low incidence of enterocolitis in this series is the systematic postoperative use of irrigations of the colon with saline in all patients. These five patients have been followed-up for growth, development, bowel habit and continence. Follow-up has ranged from 15 to 62 months (mean = 32.2 +/- 19.2 months). Presently, all patients in this series have full enteral feeding and one to three bowel movements per day, with formed or semiformed stools. No patients is incontinent of stool. The patient's body weights (74 to 93%) and heights (89 to 92%) for their age were below average (four patients) or within normal range (one patient). Hemoglobin levels are within normal range in all patients. One patient has iron deficiency and another one has serum ferritin concentration below normal. Three patients have folic acid deficiency. Vitamin B12 absorption is normal in all patients. Although we can not conclude this is a better procedure than others, with is use we have obtained satisfactory results, with an excellent survival, scanty morbidity, a rapid return of bowel function and continence, and an acceptable physical development. During long-term follow-up, patients mus be evaluated for iron and folic acid deficiency.

Child↗
PubMed1982

9-methyl pteroylglutamic acid, a synthetic analogue of folic acid: its effects on hexosamine levels in fetal rat limbs and other fetal tissues.

Pregnant rats were administered the teratogen and synthetic analogue of folic acid, 9-methyl pteroylglutamic acid, on the 11th day of gestation and placed on a semisynthetic diet containing the antagonist but lacking the vitamin until the 14th gestational day. This transitory maternal folic acid deficiency results in multiple congenital skeletal malformations. Control animals were administered a folic acid-supplemented regimen. Hexosamine levels were measured in fetal tissues, i.e. limbs, livers, and yolk sacs, in order to monitor the accumulation of a primary constituent of the extracellular matrix, i.e. glycosaminoglycans. Fetal tissues were obtained for hexosamine analysis on the 16th and 18th days of gestation. The teratogenic and transitory folic acid-deficient regimen resulted in (1) a significant reduction in the accumulation of hexosamine in fetal limbs by the 16th day of gestation, and (2) a significant increase in the accumulation of hexosamine in fetal livers by the 16th day of gestation. The regimen was observed to have had no effect on hexosamine accumulation by the yolk sac. Furthermore, no significant effect on hexosamine accumulation from the 16th to the 18th day of gestation was observed in any of the tissues studied.

Animals↗
PubMed1978

Avoidance behavior in folate--deficient rats.

The effects of folate deficiency in post-weanling male rats in an active avoidance learning test were studied. Ingestion of a folate-free diet for 3 weeks markedly decreased serum and erythrocyte folate concentrations but had only a slight effect on growth rate. The decrease in blood folates was correlated with an increase in the number of trials necessary to reach criterion in the learning test. There was no motor impairment since the mean escape latency was the same in control and folate-deficient animals. These results suggest that folic acid deficiency started at weaning could be responsible for learning impairment.

Animals↗